SOCS1 可消除 IFN 对丙型肝炎病毒复制的抗病毒作用。
SOCS1 abrogates IFN's antiviral effect on hepatitis C virus replication.
机构信息
MOH Key Laboratory of Systems Biology of Pathogens, Institute of Pathogen Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
出版信息
Antiviral Res. 2013 Feb;97(2):101-7. doi: 10.1016/j.antiviral.2012.12.001. Epub 2012 Dec 10.
Abstract
Suppressor of cytokine signaling 1 (SOCS1) and suppressor of cytokine signaling 3 (SOCS3) have been thought to block type I interferon (IFN) signaling. We have previously reported that SOCS3 suppresses HCV replication in an mTOR-dependent manner. However, the relationship between SOCS1 and HCV replication remains unclear. Here, we found that overexpression of SOCS1 alone did not have an effect on HCV RNA replication. However, suppression of HCV replication by IFN-α was rescued by SOCS1 overexpression. The upregulation of HCV replication by SOCS1 overexpression in the presence of IFN is likely a result of the impairment of IFN signaling by SOCS1 and subsequent induction of ISGs. Knockdown of SOCS1 alone with specific shRNA enhanced the antiviral effect of IFN compared with negative control. Thus, SOCS1 acts as a suppressor of type I IFN function against HCV.
摘要
细胞因子信号转导抑制因子 1（SOCS1）和细胞因子信号转导抑制因子 3（SOCS3）被认为可以阻断 I 型干扰素（IFN）信号。我们之前的研究表明，SOCS3 通过 mTOR 依赖性方式抑制 HCV 复制。然而，SOCS1 与 HCV 复制之间的关系尚不清楚。在这里，我们发现 SOCS1 的过表达本身并不影响 HCV RNA 的复制。然而，IFN-α 对 HCV 复制的抑制作用可以被 SOCS1 的过表达所挽救。在 IFN 存在的情况下，SOCS1 的过表达上调 HCV 复制可能是由于 SOCS1 损害了 IFN 信号转导，随后诱导了 ISGs。单独用特异性 shRNA 敲低 SOCS1 可增强 IFN 的抗病毒作用，与阴性对照相比。因此，SOCS1 是一种针对 HCV 的 I 型 IFN 功能的抑制剂。
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